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a(MESH:Microglia)

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Entity

Name
Microglia
Namespace
mesh
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/mesh-names.belns

Appears in Networks 11

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0

Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation v1.0.0

Amelioration of Experimental Autoimmune Encephalomyelitis by Anatabine v1.0.0

Anti-aggregant tau mutant promotes neurogenesis v1.0.0

Clearance systems in the brain-implications for Alzheimer disease. v1.0.1

Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

Extracellular Tau and Its Potential Role in the Propagation of Tau Pathology v1.0.0

Inflammasome Involvement in Alzheimer’s Disease v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

In-Edges 19

a(CHEBI:Anatabine) decreases a(MESH:Microglia) View Subject | View Object

In addition, anatabine markedly decreased the Iba1 immunostaining in the spinal cord of EAE mice showing that anatabine reduces the infiltration of macrophage/ microglia in the spinal cord of EAE mice (Fig. 10) PubMed:23383175

Appears in Networks:
Annotations
MeSH
Spinal Cord
MeSH
Encephalomyelitis

a(CHEBI:Anatabine) decreases tloc(a(MESH:Microglia), fromLoc(GO:"extracellular region"), toLoc(MESH:"Spinal Cord")) View Subject | View Object

In addition, anatabine markedly decreased the Iba1 immunostaining in the spinal cord of EAE mice showing that anatabine reduces the infiltration of macrophage/ microglia in the spinal cord of EAE mice (Fig. 10) PubMed:23383175

Appears in Networks:
Annotations
MeSH
Spinal Cord
MeSH
Encephalomyelitis

a(GO:"myelin sheath") negativeCorrelation a(MESH:Microglia) View Subject | View Object

A statistically significant positive correlation was observed between the amount of GFAP and Iba1 burden in the spinal cord (Pearson correlation = 0.612, P,0.002) whereas negative correlations were observed between the GFAP burden and the Luxol fast blue burden (Pearson correlation =20.525, P= 0.007), and between the IBa1 burden and the Luxol fast blue burden (Pearson correlation =20.609, P =0.001) suggesting that astrogliosis and microgliosis are associated with the loss of myelin in the spinal cord PubMed:23383175

Appears in Networks:
Annotations
MeSH
Spinal Cord

a(MESH:Astrocytes) positiveCorrelation a(MESH:Microglia) View Subject | View Object

A statistically significant positive correlation was observed between the amount of GFAP and Iba1 burden in the spinal cord (Pearson correlation = 0.612, P,0.002) whereas negative correlations were observed between the GFAP burden and the Luxol fast blue burden (Pearson correlation =20.525, P= 0.007), and between the IBa1 burden and the Luxol fast blue burden (Pearson correlation =20.609, P =0.001) suggesting that astrogliosis and microgliosis are associated with the loss of myelin in the spinal cord PubMed:23383175

Appears in Networks:
Annotations
MeSH
Spinal Cord

path(MESH:Encephalomyelitis) increases a(MESH:Microglia) View Subject | View Object

Globally, Iba1 immunostaining is significantly increased in the spinal cord of EAE mice compared to control nonimmunized mice (Fig. 10) PubMed:23383175

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) negativeCorrelation act(a(MESH:Microglia)) View Subject | View Object

In controls and anti-aggregant TauRDΔKPP slices, the microglia were mainly in the ramified form, in contrast to the pro-aggregant TauRDΔK slices where microglia were more of the reactive form (Fig 3b) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) decreases a(MESH:Microglia) View Subject | View Object

Total numbers of Iba1 positive microglial cells were reduced to 50% in anti-aggregant TauRDΔKPP slices when compared to controls (Fig. 3c, bar 2) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) causesNoChange act(a(MESH:Microglia)) View Subject | View Object

The antiaggregant TauRDΔKPP slices had ramified form of microglia with 6-7 branches on an average indicating that the microglial cells were in their normal physiologically active form and there is no sign of inflammation (Fig 3d, bars 1 and 2). PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) positiveCorrelation act(a(MESH:Microglia)) View Subject | View Object

In controls and anti-aggregant TauRDΔKPP slices, the microglia were mainly in the ramified form, in contrast to the pro-aggregant TauRDΔK slices where microglia were more of the reactive form (Fig 3b) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) increases a(MESH:Microglia) View Subject | View Object

The opposite result was observed in the pro-aggregant TauRDΔK slices where the microglial number was increased by 100% compared to controls (Fig. 3c, bar 3) PubMed:29202785

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) positiveCorrelation act(a(MESH:Microglia)) View Subject | View Object

On the contrary, microglia in proaggregant TauRDΔK slices, were increased in number and were also observed with 2-3 branches on an average compared to age-matched controls and also the antiaggregant TauRDΔKPP slices (Fig. 3d, bar 3). This indicates that in the pro-aggregant TauRDΔK slices the microglia are in a reactive form, indicating that there is also enhanced inflammation PubMed:29202785

Appears in Networks:

a(CHEBI:rosiglitazone) increases act(a(MESH:Microglia)) View Subject | View Object

Rosiglitazone, a highaffinity agonist for PPARγ, can clear Aβ by activating microglia and promoting its phagocytosis via increasing the levels of CD36, a receptor expressed in it (Escribano et al. 2010) PubMed:29626319

Appears in Networks:

p(HGNC:TREM2, var("p.Arg47His")) decreases act(a(MESH:Microglia)) View Subject | View Object

However, due to the presence of the R47H mutation in AD, TREM2 cannot effectively recognize the lipid ligands and then fails to activate microglia, which leads to Aβ deposition (Jiang et al. 2014a; Jiang et al. 2013) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") increases act(a(MESH:Microglia)) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta polypeptide 42") positiveCorrelation act(a(MESH:Microglia)) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:"peroxisome proliferator activated receptor signaling pathway") increases act(a(MESH:Microglia)) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:"positive regulation of advanced glycation end-product receptor activity") increases act(a(MESH:Microglia)) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(complex(GO:"NF-kappaB complex")) increases act(a(MESH:Microglia)) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(MESH:"I-kappa B Proteins", pmod(Ph)) increases act(a(MESH:Microglia)) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 25

a(MESH:Microglia) regulates deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

By contrast, the parenchyma of the CNS is devoid of lymphatic vasculature2; in the brain, removal of cellular debris and toxic molecules, such as amyloid-β peptides, is mediated by a combination of transcellular transport mechanisms across the blood−brain and blood−cerebrospinal fluid (CSF) barriers7–9, phagocytosis and digestion by resident microglia and recruited monocytes and/or macrophages10,11, as well as CSF influx and ISF efflux through a paravascular (glymphatic) route12–14 PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

a(MESH:Microglia) increases a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") View Subject | View Object

We next tested the impact of anatabine on STAT3 and p65 NFkB phosphorylation induced by a 24 h treatment with LPS on human microglial cells, a cell type known to express alpha7-nicotinic acetylcholine receptor subtype (Suzuki et al., 2006) PubMed:23178521

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell

a(MESH:Microglia) positiveCorrelation a(MESH:Astrocytes) View Subject | View Object

A statistically significant positive correlation was observed between the amount of GFAP and Iba1 burden in the spinal cord (Pearson correlation = 0.612, P,0.002) whereas negative correlations were observed between the GFAP burden and the Luxol fast blue burden (Pearson correlation =20.525, P= 0.007), and between the IBa1 burden and the Luxol fast blue burden (Pearson correlation =20.609, P =0.001) suggesting that astrogliosis and microgliosis are associated with the loss of myelin in the spinal cord PubMed:23383175

Appears in Networks:
Annotations
MeSH
Spinal Cord

a(MESH:Microglia) negativeCorrelation a(GO:"myelin sheath") View Subject | View Object

A statistically significant positive correlation was observed between the amount of GFAP and Iba1 burden in the spinal cord (Pearson correlation = 0.612, P,0.002) whereas negative correlations were observed between the GFAP burden and the Luxol fast blue burden (Pearson correlation =20.525, P= 0.007), and between the IBa1 burden and the Luxol fast blue burden (Pearson correlation =20.609, P =0.001) suggesting that astrogliosis and microgliosis are associated with the loss of myelin in the spinal cord PubMed:23383175

Appears in Networks:
Annotations
MeSH
Spinal Cord

act(a(MESH:Microglia)) negativeCorrelation p(HBP:"Tau isoform F (441 aa)", var("p.Ile277Pro"), var("p.Ile308Pro"), var("p.Lys280del")) View Subject | View Object

In controls and anti-aggregant TauRDΔKPP slices, the microglia were mainly in the ramified form, in contrast to the pro-aggregant TauRDΔK slices where microglia were more of the reactive form (Fig 3b) PubMed:29202785

Appears in Networks:

act(a(MESH:Microglia)) positiveCorrelation p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) View Subject | View Object

In controls and anti-aggregant TauRDΔKPP slices, the microglia were mainly in the ramified form, in contrast to the pro-aggregant TauRDΔK slices where microglia were more of the reactive form (Fig 3b) PubMed:29202785

Appears in Networks:

act(a(MESH:Microglia)) positiveCorrelation p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) View Subject | View Object

On the contrary, microglia in proaggregant TauRDΔK slices, were increased in number and were also observed with 2-3 branches on an average compared to age-matched controls and also the antiaggregant TauRDΔKPP slices (Fig. 3d, bar 3). This indicates that in the pro-aggregant TauRDΔK slices the microglia are in a reactive form, indicating that there is also enhanced inflammation PubMed:29202785

Appears in Networks:

a(MESH:Microglia) decreases a(CHEBI:"amyloid-beta", loc(MESH:"Extracellular Fluid")) View Subject | View Object

Specifically, ISF Aβ can be taken up by microglia and astrocytes, whereas perivascular Aβ can be degraded by vascular smooth muscle cells, perivascular macrophages, and astrocytes PubMed:26195256

Appears in Networks:

act(a(MESH:Microglia)) increases bp(HBP:Neurodegeneration) View Subject | View Object

Activated microglia has a double effect on AD progression (Li et al. 2014). On the one hand, they can release some proinflammatory cytokines, stimulating inflammatory response and ultimately leading to neuronal injuries and death PubMed:29626319

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:Microglia) increases bp(GO:"immune response") View Subject | View Object

Microglia, one type of glial cells, the equivalent of the macrophages that exist in the brain and spinal cord, is the first and also the main line of immune defense in CNS PubMed:29626319

Appears in Networks:
Annotations
MeSH
Central Nervous System

act(a(MESH:Microglia)) increases bp(GO:"cytokine production involved in inflammatory response") View Subject | View Object

Activated microglia has a double effect on AD progression (Li et al. 2014). On the one hand, they can release some proinflammatory cytokines, stimulating inflammatory response and ultimately leading to neuronal injuries and death PubMed:29626319

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases bp(GO:"inflammatory response") View Subject | View Object

Activated microglia has a double effect on AD progression (Li et al. 2014). On the one hand, they can release some proinflammatory cytokines, stimulating inflammatory response and ultimately leading to neuronal injuries and death PubMed:29626319

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases bp(GO:phagocytosis) View Subject | View Object

On the other hand, they may show beneficial effects via facilitating aberrant protein clearance by means of microglial migration to the damaged, aberrant area, and phagocytosis of unnecessary materials in the early stages of AD PubMed:29626319

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:Microglia) increases bp(GO:phagocytosis) View Subject | View Object

Microglial cells, the key immune cells of the brain, play an important part in the phagocytosis of Aβ PubMed:29626319

Appears in Networks:

a(MESH:Microglia) increases p(HGNC:MAPT) View Subject | View Object

N2a cells over-expressing tau (Wang et al., 2017) and microglia also release tau in an exosome-dependent manner PubMed:29238289

Appears in Networks:
Annotations
MeSH
Blood
MeSH
Cerebrospinal Fluid

a(MESH:Microglia) increases p(HGNC:NLRP3) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

a(MESH:Microglia) increases p(HGNC:P2RX7) View Subject | View Object

P2X7 expressed by microglial cells will also activate the NLP3 inflammasome [30, 32] and the expression of P2X7 is likely to be increased in AD brains [35]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph

a(MESH:Microglia) increases p(HGNC:TLR4) View Subject | View Object

Pattern recognition receptors such as the TLR4 receptor are expressed in the brain’s own immune cells like microglia and astrocytes that induce inflammation via cytokine secretion [38]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Brain
MeSH
Alzheimer Disease
NeuroMMSigDB
Toll like receptor subgraph

a(MESH:Microglia) regulates act(p(HBP:"Tau oligomers", var("p.Lys280del"))) View Subject | View Object

We reasoned that microglia and other cell types in the hippocampus might act as mediators for the cytotoxicity caused by TauRDΔK oligomers, which could explain why cytotoxicity was not observed in the cell culture systems. PubMed:28528849

Appears in Networks:

act(a(MESH:Microglia)) increases p(HGNC:TNF) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases p(HGNC:IL1B) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases p(HGNC:IL6) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases p(HGNC:CXCL8) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases bp(GO:"neuron death") View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) positiveCorrelation a(CHEBI:"amyloid-beta polypeptide 42") View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.